Human genetic data have associated angiotensin-converting enzyme (ACE) with Alzheimer
disease (AD), and purified ACE has been reported to cleave synthetic amyloid β-protein (Aβ)
in vitro. Whether deficiency in ACE activity, arising from genetic alteration or
pharmacological inhibition, can decrease Aβ degradation and allow Aβ accumulation in
intact cells is unknown. We cloned ACE from human neuroblastoma cells and showed that it
had posttranslational processing and enzymatic activity typical of the endogenous protease …